Uploaded byDr. Kanwal Deep Singh Lyall
Sexually transmitted diseases
This document discusses sexually transmitted diseases (STDs). It defines STDs as communicable diseases predominantly transmitted through sexual contact and caused by bacteria, viruses, fungi or parasites. It then discusses factors influencing STDs, populations at risk, common clinical presentations including genital ulcers and discharge, and various STDs like syphilis, chlamydia, herpes, HIV and hepatitis B and C. It also covers the etiology, pathogenesis, signs and symptoms, complications and methods of laboratory diagnosis for major STDs.
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Sexually transmitted diseases
- 1. Sexually Transmitted Diseases Dr. KanwalDeep S. Lyall
- 2. The sexually transmitteddiseases are a group of communicable diseases that are transmitted predominantly by sexual contact and caused by a wide range of bacterial, viral, protozoal and fungal agents
- 3. Biological factors Socialand behavioral factors Asymptomatic nature of STDs. Poverty and marginalization Lag time between infection and complications. Substance abuse, sex work Gender and age Access to health care Sexuality and secrecy Changing sexual behaviors and sexual norms Factors influencing STDsFactors influencing STDs
- 4. Those at riskfrom STDs • Sex workers, male & female • Clients of sex workers • Homosexuals • Injecting drug users & their partners • Frequent travelers
- 5. Common STD syndromes •Urethritis(males) •Epididymitis •Lower genital tract infections: females Cystitis/ urethritis Mucopurulent cervicitis Vulvovaginitis Bacterial vaginosis •Acute PID •Ulcerative lesions of genitalia •Proctitis •Enteritis, enterocolitis, proctocolitis •Acute arthritis •Genital and anal warts •AIDS •Viral hepatitis •Neoplasias •Scabies •Pubic lice
- 6.
- 7. Male genital tractFemale genital tract
- 8.
- 9. STDs etiology Anatomy Clinical Presentation Bacteria VirusFungi Parasites Lower genital Tract inflections Upper genital tract infections Genital discharge Genital ulcers No genital lesion but only systemic manifestations miscellaneou
- 10.
- 11. Bacterial • Treponema pallidum •N.gonorrhoea • H. ducreyi • Chlamydia trachomatis • Calymmatobacterium granulomatous • Mobiluncus curtisii • Ureaplasma urealyticum, Mycoplasma hominis • Gardenella vaginalis • Acinetobacter • Bacteroidis • Campylobacter • Group B streptococci
- 12. Viral • Herpes simplex •Hepatitis B • Hepatitis C • Molluscum contagiosum virus • HIV 1,2
- 13. Fungi • Candida Protozoa • Trichomonasvaginalis • Leishmania donovani • Entamoeba histolytica • Giardia intestinalis
- 14.
- 15. Genital ulcers Painless ulcersPainful ulcers Syphilis Treponema pallidum LGV Chlamydia trachomatis Donovanosis C. granulomatis Chancriod Haemophilus ducreyi Herpes genitalis HSV type 2
- 16. Gonorrhea Neisseria gonorrhoeae Trichomonasvaginitis Trichomonas vaginalis Non-gonococcal urethritis •C. Trachomatis •Ureaplasma urealyticum •Mycoplasma genitalium •M. hominis •Acinetobacter lwoffi •Bacteroides urealyticus •Candida albicans •Torulopsis glabrata Bacterial vaginosis •Mobiluncus curtisii •M.mulieris •Mycoplasma hominis •Gardenella vaginalis •Bacteroides spp. Genital discharge
- 17. No genital lesionbut only systemic manifestations HIV-1 & HIV-2 AIDS Hepatitis B HBV Hepatitis C HCV
- 18. Miscellaneous • Shigella spp. •Campylobacter spp. • Group B streptococci • Human herpes virus 5 (CMV) • Human papilloma viruses • Molluscum contagiosum virus • Entamoeba histolytica • Giardia intestinalis
- 19.
- 20. Route of entry •Sexualroute •Vaginal •Anal •Oral •Autoinfection Genital herpes, MCV •Vertical route Congenital syphilis,HIV •Direct trauma H ducreyi •Blood transfusion Syphilis, HIV, hepatitis B
- 21. General mechanism • Entry •Attachment • Penetration • Inflammatory response • Clinical signs & symptoms
- 22. Factors contributing to virulence Host/localfactors Organism’s virulence factors pH Pili Secretions OMP Mucosal/skin breach IgA proteases Immune status LPS Local infections Toxins
- 23. Syphilis (painless) • Sexualcontact • Entry through abrasions • Multiplication at the site of entry • IP 9-90days • Primary lesion → chancre LN enlargement healingx10-40days→ → • 1-3mnths secondary syphilis (most infectious)→ • Wide spread multiplication & dissemination in blood • Rash, mucus patches, condylomata • Ophthalmic, osseous, meningial • 4-5yrs quiescence latent syphilis→ → • Tertiary syphilis CVS & CNS involvement→ • Quaternary syphilis tabes dorsalis, GPI→
- 24. Chancroid (H Ducreyi-painful) •Potent cytolethal distending toxin • Generation and slow healing of ulcers. • Facilitates HIV transmission. • Macrophages in lesions have significantly increased expression of CCR5 and CXCR4 • CCR5 and CXCR4 main co-receptors essential for HIV entry. • Presence of cells with up-regulated HIV-1 co-receptors • Disruption of mucosal and skin barriers, • An environment that facilitates the acquisition of HIV- 1 infection.
- 25. LGV (C. trachomatis-painless) •Sexual contact • IP 3-5weeks • Primary lesion papulovesicular lesion on external genitals→ • 2 weeks later seconday stage spreads to regional LNs→ → • men inguinal/women intrapelvic & pararectal→ → • LNs enlarge suppurate become adherent to skin→ → • Break down to from sinuses discharging pus • Involvement of other organs • Tertiary stage chronic sequels scarring & lymphatic→ → blockage • Rectal strictures & elephantiasis of vulva in women
- 26. Herpes simplex virus2 - painful • Close contact/venereal • Entry through defects in skin/mucosa • Local multiplication with cell to cell spread • Entry into cutaneous nerve fibers transported intra-→ axonally to ganglia replication→ • Virus remains latent in ganglia (sacral) • Reactivated periodically • Thin walled, umbilicated vesicles • Roof breaks down tiny superficial ulcers→ • Heals without scarring
- 27. Calymmatobacterium granulomatis • Painless •Normally present in the gut flora • Autoinoculation or sexual contact. • Penetration→ inflammatory reaction, • Destruction of the infected tissue. • mainly intracellularly inside tissue macrophages (Donovan bodies). • Painless papules→ ulcers • Superinfection
- 29. HIV • Main damageto CD+ T lymphocytes decrease in No.→ • T4:T8 (helper : suppressor) cell ratio reversal • Decreased production of IL-2, γ-IF & other lymphokines • Decreased response to new antigens • Polyclonal activation of B lymphocytes • Hypergammaglobulinemia • Mainly IgG & IgA (IgM in infants & children) • Useless Ig • Immunosuppression • Opportunistic infections
- 30. •Parenteral,Peri- natal,Sexual,Others •Exact mechanismnot known •Most studies suggest- virus is not cytopathic directly. •Infectious virion attaches to cell and uncoats •In nucleus partially d/s viral genome convert to cccDNA •This serves as template for all viral transcripts •Pregenome RNA becomes encapsulated with HBcAg •Minus and incomplete plus DNA strand is synthesized •Cores bud, acquiring HBsAg containing envelope & exits Hepatitis B
- 31. Hepatitis C • Sexualtransmission • Injecting drug use • Occupational exposure to blood • Perinatal • Household transmission • HCV RNA can be detected within days after exposure, often 1-4 weeks before enzymes ↑ • Viremia peaks in 8-12 weeks of infection • HCV infection leads to hepatic inflammation & Steatosis • Persistent HCV infection leads to Hepatic fibrosis & risk↑ of HCC
- 32.
- 33. Disease Causative organism Incubation period Lesion siteof lesion Clinical features Lymph nodes Syphilis Treponema pallidum 9-90 days Hard chancre (1° syphilis) genital M: undersurfa ce of prepuce, penis F: labia majora, minora, clitoris, cervix, vagina extragenit al lips, breast, finger tips •clean •non tender •single ulcer •heals spontaneo usly within 4-6 wks •regional lap adjacent to chancre •ln are firm, discrete, rubbery, non- tender, non- suppurativ e
- 34. Disease Causative organism Incubatio n period Lesionsite of lesion Clinical features Lymph nodes chancroid H.Ducreyi 2-7 days soft chancre genital only m: undersurfa ce of prepuce, glans penis, shaft of penis f: chiefly labia majora, minora, fourchette •necrotic, dirty, surrounde d by erythemato us halo •tender •multiple ulcers •may burst to form a sinus or may heal spont. to induce breif scars. lymphaden itis absent
- 35. Disease Causative organism Incubatio n period Lesionsite of lesion Clinical features Lymph nodes LGV Chlamydia trachomatis 6-42 days primary genital lesion M: glans penis, prepuce or shaft of penis F: rarely lymphatics Groin, genital, rectal •small herpetifor m lesion •may be ulcer, papule, vesicle or pustule •single •painless •non indurate •transitory •painful inguinal lap •tendency to suppurate •genito- anorectal syndrome •usually in female – anorectal ulceration
- 36. Disease Causativ e organis m Incubati on period Lesion siteof lesion Clinical features Lymph nodes Genital herpes HSV 1 & 2 2-21 days - M: Glans, shaft of penis F: Labia, vagina or cervix, clitoris, May spread to surroundi ng skin •small vesicles arranged in group with erythemat backgrou nd •veicles rupture to form multiple painful ulcers •75% patients •non- suppurati ve •inginual, pelvic, femoral lap
- 37. Disease Causative organism Incubati on period Lesio n site oflesion Clinical features Lymph nodes Donovaniasis or granuloma inguinale calymmato- bacterium granulomatis 3-90 days - Moist stratified squamous epithelial - Primary target Others: Genitalia, thigh, groin, perineum •non indurated •non tender •single, elevated, granuloma tous ulcer •ulcerated lesions are irregular in shape with rolled border on beefy red, cobbleston e base •s/c granuloma s, not involving ln, called as pseudo lymphadenitis absent
- 38. Hepatitis B Acute Infection •IP-1-4 months •Clinically- Flu like symptoms •Symptoms generally disappear after 1-3 months •Severe if co infection of Hepatitis D & underlying condition such as ALD Fulminant Hepatitis •Is rare ( 0.1%- 1%) •Rapidly progressing Acute hepatitis with signs of liver failure •More common with co-infection with Hep –D Chronic Hepatitis •6 months of persistent HBV infection •Symptoms are non specific
- 39. Acute Hepatitis •Flu Likesymptoms •IP-7 weeks •Liver specific enzymes↑ Fulminant Hepatitis •Signs of liver failure Chronic Hepatitis •50%- 85% persons •Can progress to Cirrhosis. Hepatocellular Carcinoma •Primary HCC late complication of chronic HCV infection •Sudden worsening of prior symptoms with signs of Cirrhosis Hepatitis C
- 40. HIV 1. Acute infection 2.Asymptomatic or latent infection 3. PGL 4. ARC 5. AIDS 6. DEMENTIA 7. Pediatric AIDS
- 41.
- 42. Males Females infants Urethral stricture PIDCongenital syphilis Acute & chronic epididymitis Infertility Ophthalmia neonatorum Infertility Chronic abdominal pain Blindness Penile cancer Ectopic pregnancy Cancer of cervix uteri
- 43.
- 44. Precautions 1. Use ofgloves while taking samples 2. Sample should be collected before start of antibiotics 3. No antiseptics should be used while collecting specimen 4. Clean area with gauge soaked in normal saline
- 45.
- 46.
- 47. Specimen Container Patientpreparation Special instructions Bartholin cyst Anaerobic transport Disinfect skin before collection Aspirate fluid; consider chlamydia & GC culture Cervix Swab moistened with Stuart’s or Amies medium Remove mucus before collection Do not use lubricant on speculum; use viral/chlamydial transport medium, if necessary; swab deeply into cervical canal Cul-de-sac Anaerobic transport Submit aspirate Endometrium Anaerobic transport Surgical biopsy or transcervical aspirate via sheathed catheter Urethra Swab moistened with Stuart’s or Amies medium Remove exudate from urethral opening Collect discharge by massaging urethra against pubic symphis or insert flexible swab 2-4 cm into urethra & rotate for 2 secs; at
- 48. Specimen Container Patientpreparation Special instructions Vagina Swab moistened with Stuart’s or Amies medium Remove exudate Swab secretions & mucus membrane of vagina
- 49.
- 50. Specimen Container Patientpreparation Special instructions Prostate Swab moistened with Stuart’s or Amies medium or sterile screw-cap tube Clean glans with soap & water Collect secretions on swab or in tube Urethra Swab moistened with Stuart’s or Amies medium Insert flexible swab 2-4 cm into urethra & rotate for 2 secs or collect discharge
- 51. Urine Initial flow ratherthan the mid stream collected Blood Collected aseptically in plain vials
- 52. Collection of sampleto detect T.pallidum • Cleanse area around ulcer with moistened swab • Remove scab if present • Squeeze lesion to obtain serous fluid • Collect drop on cover slip-invert it on slide • Deliver immediately
- 53. Collection of sampleto detect C.granulomatis • Cleanse area around ulcer with moistened swab • Pinch off some tissue from edge or base of lesion • Crush between two slides • Deliver immediately • If delay-fix with methyl alcohol (1- 2mnts)
- 54. Specimen Direct Culture Non-culture Wetmount Gram stain Wright Giemsa Staining Dark Ground Illumination Electron Microscopy media Colony Characteristics
- 55.
- 56. • T. vaginalis •Pear shaped, ovoid nucleus at the anterior end, & cytostome • 3-5 anterior flagella which are free • Axostyle runs down the middle of the body and ends in pointed tail like extremity • Jerky motility
- 57. • Candida • Yeastlike cells and pseudohyphae
- 59. • Mobiluncus • Cluecells (epithelial cells with surface covered with adherent bacilli)
- 61.
- 62. • Gram negative,intracellular, diplococci, kidney shaped, with adjacent sides concave → N. gonorrhoeae
- 63. • Gram negative,ovoid, bacillus, bipolar staining, they may be arranged in small groups or whorls or in parallel chains giving a ‘school of fish’ or ‘rail road track appearance’ → H. ducreyi
- 64. • Gram positivewith budding yeast cells, pseudohyphae candida→
- 65. • Gardenella vaginalis •Clue cells-epithelial cells with adhering polymorphic bacteria
- 66. Wright Giemsa Staining •Donovan bodies (round coccobacilli 1x2 µm) present within cystic spaces in cytoplasm of mononuclear cells. • Capsule appears as dense acidophilic zone resembling a ‘closed safety pin’ • Elementary bodies (Miyagawa’s granulocorpuscles) C. trachomatis→ • Multinucleated Giant cells and I/N inclusion bodies HSV→ • Molluscum bodies MCV→
- 67.
- 68. culture MNYC Or Thayer Martin medium 2BA MacConkeyCMB Aerobically & anaerobically 37° C x 24hrs 37° C x 24hrs s/c at 24hrs 48hrs 72hrs 37° C x 48hrs in moist CO2 Enriched atmosphere Small, raised, grey, shiny clonies oxidase positive GNDC N. gonorrhoeae S.Pyogenes S.Aureus C.Perfringens Proteus Enterococci E.Coli Bacteroides
- 69. Gram stain GNDC CBBY&PH Inclusion bodies
- 70. Gram stain GNDC CBBY&PH Inclusion bodies CA
- 71. Gram stain GNDC CBBY&PH Inclusion bodies CA colonies
- 72. Gram stain GNDC CBBY&PH Inclusion bodies CA Small, grey, translucent, glistening colonies
- 73. Gram stain GNDC CBBY&PH Inclusion bodies CA Small, grey, translucent, glistening Small, round, Translucent, convex, fine, granular colonies
- 74. Gram stain GNDC CBBY&PH Inclusion bodies CA Small, grey, translucent, glistening Small, round, Translucent, convex, fine, granular colonies H ducreyi N gonorrhoeae
- 75. Gram stain GNDC CBBY&PH Inclusion bodies CA Small, grey, translucent, glistening Small, round, Translucent, convex, fine, granular colonies H ducreyi N gonorrhoeae Agglutination with antisera Oxidase + Fermentation of glucose only
- 76. Gram stain GNDC CBBY&PH Inclusion bodies CA Small, grey, translucent, glistening Small, round, Translucent, convex, fine, granular colonies H ducreyi N gonorrhoeae Agglutination with antisera Oxidase + Fermentation of glucose only SDA
- 77. Gram stain GNDC CBBY&PH Inclusion bodies CA Small, grey, translucent, glistening Small, round, Translucent, convex, fine, granular colonies H ducreyi N gonorrhoeae Agglutination with antisera Oxidase + Fermentation of glucose only SDA Creamy white colonies with yeast odour
- 78. Gram stain GNDC CBBY&PH Inclusion bodies CA Small, grey, translucent, glistening Small, round, Translucent, convex, fine, granular colonies H ducreyi N gonorrhoeae Agglutination with antisera Oxidase + Fermentation of glucose only SDA Creamy white colonies with yeast odour Candida
- 79. Gram stain GNDC CBBY&PH Inclusion bodies CA Small, grey, translucent, glistening Small, round, Translucent, convex, fine, granular colonies H ducreyi N gonorrhoeae Agglutination with antisera Oxidase + Fermentation of glucose only SDA Creamy white colonies with yeast odour Candida GTT Chlamydiospores
- 80. Gram stain GNDC CBBY&PH Inclusion bodies CA Small, grey, translucent, glistening Small, round, Translucent, convex, fine, granular colonies H ducreyi N gonorrhoeae Agglutination with antisera Oxidase + Fermentation of glucose only SDA Creamy white colonies with yeast odour Candida GTT Chlamydiospores Contd..
- 81.
- 82. Donovan bodies Elementary bodies C trachomatis Cgranulomatis
- 83. Donovan bodies Elementary bodies Intranuclear IB Tissue culture CAM HSV Ctrachomatis C granulomatis
- 84.
- 85. Lab diagnosis ofsyphilis Serological tests for detection of antibody in serum/CSF Microscopy
- 86. Lab diagnosis ofsyphilis Primary & secondary syphilis DGM, DFA-TP Serological tests for detection of antibody in serum/CSF Microscopy
- 87. Lab diagnosis ofsyphilis Primary & secondary syphilis DGM, DFA-TP Serological tests for detection of antibody in serum/CSF Microscopy
- 88. Lab diagnosis ofsyphilis Primary & secondary syphilis DGM, DFA-TP Serological tests for detection of antibody in serum/CSF STS (Cardiolipin Ag) •Wasserman’s compliment fixation test •Kahn’s test •VDRL •RPR •TRUST Microscopy
- 89. Lab diagnosis ofsyphilis Primary & secondary syphilis DGM, DFA-TP Serological tests for detection of antibody in serum/CSF STS (Cardiolipin Ag) •Wasserman’s compliment fixation test •Kahn’s test •VDRL •RPR •TRUST Group specific tests (Reiter’s strain) RPCF Microscopy
- 90. Lab diagnosis ofsyphilis Primary & secondary syphilis DGM, DFA-TP Serological tests for detection of antibody in serum/CSF STS (Cardiolipin Ag) •Wasserman’s compliment fixation test •Kahn’s test •VDRL •RPR •TRUST Group specific tests (Reiter’s strain) RPCF Specific tests using pathogenic to treponeme (Nichol’s strain) •TPI •FTA •FTA-ABS •TPHA •EIA Microscopy
- 91. • Clinical activityof syphilis: VDRL, RPR • Monitoring response to treatment : Reagin Tests • Confirmation of diagnosis & Identifying BFP: TPHA, FTA- ABS • Negative TPHA=100% negative syphilis • IgM +ve=active disease, congenital syphilis
- 92. HIV 1. Immunological tests •TLC/DLC • CD4+T cell count (≤200/mm3 ) • T4:T8 cell ratio reversal • TCP • Raised IgG & IgM levels • Decreased CMI (skin tests)
- 93. Specific tests forHIV • Ag detection P24 earliest detected→ • Virus isolation • PCR • Antibody detection • Western Blot method confirmation→
- 94. Hepatitis B Infections withHBV is associated with characteristic pattern of Hepatitis antigen & antibodies • Acute Hepatitis • detection of HBsAg & IgM anti- HBc • HBeAg and HBV DNA present during Replicative Phase • HBsAg is serological hallmark - appears 1-10 weeks after exposure, becomes undetectable after 4-6 months • HBeAg is a marker of HBV replication • HBcAg is an intracellular Ag, not detected in serum • Anti- HBc Ag can be detected throughout the course of infection & its presence signifies natural infection • During recovery from acute infection anti-HBe appears first followed by anti- HBs
- 95. Hepatitis C lab diagnosisis based principally on detection of antibodies to recombinant HCV polypeptides • Serological tests • Second generation EIA-NS4, Core, and NS3 sequences • Third generation EIA includes NS5 protein and reconfiguration of the core and NS3 antigens • Sensitivity of third generation assay is 97% and can detect HCV antibody within 6-8 weeks after exposure • So-called confirmatory test are used to evaluate positive EIA these includes- RIBA recombinant immunoblot assays • RIBA detects specific antigens to which antibodies are reacting
- 96. Skin tests Frie,s test(C. Trachomatis) • Ag used : Lygranum • 0.1ml Ag inj. I.D on ventral aspect of forearm & • a control prepared from uninfected yolk sac on other forearm • 5-5 days nodule (7mm diameter )→ Ducrey’s skin test (H. Ducreyi) • Killed organism used as Ag • 0.1ml Ag inj. I/D on forearm • NS injected in other forearm as control • erythema+induration (36-48hrs) = positive result
- 97. Treatment Discharge Ulcers Urethral vaginalTransudated (Syphilis ) Non-indurated (herpes) Gonococ cal NGU Mucopur ulent (TV) Curd like (candida ) Benzathaine pen G 2.4 1.2million units I/M ODx10days Symptomatic Norflox 800mg OD Doxy 100mg BDX7- 14days Metro 200mg TDSx7 days Co-Tri ODx6 days Procaine pen G 1.2million units I/M ODx1Odays Acyclovir 200mg POx5times/dayx7 Procaine penicilli n 5.8lac with oral probenci d Erythro 500mg qidx7- 14days Or meconaz ole Doxy OD if Pen sensitive LGV Erthro 100mg BDx14days Ceftraix one
- 98. Control & Prevention •Accurate diagnosis • Effective treatment • Investigations to establish cure before resumption of sexual activity • Counseling around safe sexual practices • Partner notification • Confidentiality • STI screening for people who have unprotected sex • Serological tests for blood, organ/tissue & semen donors (syphilis, hepatitis B & C, HIV) • Serological tests for pregnant women
- 101. culture MNYC Or Thayer Martin medium 2 BA MacConkeyCMB Aerobically& anaerobically 37° C x 24hrs 37° C x 24hrs s/c at 24hrs 48hrs 72hrs 7° C x 48hrs in moist CO2 nriched atmosphere Small, raised, grey, shiny clonies oxidase positive GNDC N. gonorrhoeae
- 102. STDs Lower genital tract infections Uppergenital tract infections lesions systemic Urethritis, Cervicitis, Vaginitis Specimen collection Urethral Cervical Vaginal Bartholin’s glands Aspirate Swabs Urine Discharge M F Swabs Discharge Transport
- 103.
- 104. Lab diagnosis ofsyphilis Primary & secondary syphilis Wet film, DGM, DFA-TP Serological tests for detection of antibody in serum/CSF STS (Cardiolipin Ag) •Wasserman’s compliment fixation test •Kahn’s test •VDRL •RPR •TRUST Group specific tests (Reiter’s strain) RPCF Specific antibody to T palladium (Nichol’s strain) •TPI •FTA •FTA-ABS •TPHA •EIA Microscopy
- 105. Gram stain GNDC CBBY&PH Inclusion bodies CA Small, grey, translucent, glistening Small, round, Translucent, convex, fine, granular colonies H ducreyi N gonorrhoeae Agglutination with antisera Oxidase + Fermentation of glucose only SDA Creamy white colonies with yeast odour Candida GTT Chlamydiospores Contd..
- 106. Blood • Position thepatient • Hyperextend patient's arm. • Apply the tourniquet 3-4 inches above the selected puncture site. • Identify vein • Disinfect with 10% Povidone-Iodine in a circle of approximately 5 cm in diameter • After 2 min collect 5-10 ml blood • Plain vial
- 107. Clinical outcome of hepatitisB Acute hepatitis B Resolution HBsAg + for >6mnths Fulminant hepatitis Resolution Asymptomatic carrier state Chronic persistent hepatitis Chronic active hepatitis Extra hepatic disease: PAN, GN Cirrhosis Hepatic cell carcinoma 9% 1% 50% 90%
- 108. Hepatitis • HBsAg positive=acute/chronic/carrier • Anti HBsAg positive=immunization/good immunity/protection against hepatitis B • HbCAg – undetectable • Anti HbCAg (IgM & IgG), IgM-acute, IgG- chronic • HbeAg denotes high infectivity & active disease • Anti HbeAg denotes low infectivity • Anti HCV – Acute hep. C • HCV RNA – most sensitive & gold standard
- 109. • Early (infectious)syphilis • Time after exposure • 9-90 days Primary • 6 weeks - 6 months Secondary • (4-8 weeks after primary lesion) • £2 years (Early) Latent • Late (non-infectious) syphilis • >2 years (Late) Latent • 3-20 years Tertiary • Gummatous • Cardiovascular • Neurosyphilis • Congenital syphilis • <2 years since birth Early congenital syphilis • (includes stillbirth) • >2 years Late congenital syphilis
- 110. Factors influencing STDs •Cultural background • Sex education • Occupation • Socio economic status • Urbanization • Migration of people for want of job • Environmental factors